Elevated C-Reactive Protein Levels in Overweight and Obese Adults
January 15, 2000
Clinical Briefs
Elevated C-Reactive Protein Levels in Overweight and Obese Adults
Though previously regarded as a fairly passive storage depot, the fat compartment is now known to produce such compounds as Interleukin-6, ultimately being responsible for as much as 25% of IL-6 made each day. IL-6 is a stimulant of local and systemic inflammation, and promotes hepatic acute-phase protein generation.
CRP is an acute-phase protein predictive of risk of coronary heart disease, MI, ischemic stroke, and peripheral arterial disease. Visser and associates sought to elucidate the relationship between overweight, obesity, and serum CRP.
From the National Health and Nutrition Examination Survey (NHANES III) population, a sample (n = 16,616) of individuals had BMI measured in conjunction with CRP. Most healthy individuals have a CRP level that is undetectable (designated < 0.22 mg/dL, the lower limit of detection by currently available measurement tools); clinical elevation of CRP is considered a level > 1.00 mg/dL. Patients with disorders known to influence CRP (e.g., rheumatoid arthritis) were excluded from the trial.
Prevalence of detectable CRP levels rose as BMI increased in both genders. Frankly elevated CRP levels were 2-6 times more common amont obese individuals than their normal weight counterparts. Visser et al conclude that these data suggest a state of low-grade inflammation in overweight and obese persons.
Visser M, et al. JAMA 1999;282: 2131-2135.
Clinical Scenario: The 60-year-old woman whose ECG is shown in the Figure presented to the emergency department (ED) with shortness of breath. Can you guess why?
Interpretation: The rhythm is sinus tachycardia at a rate of 125 beats/minute. The PR and QRS intervals are normal. The QT interval may be prolonged, although it is difficult to tell for sure given the rapid rate. Marked RAD (right axis deviation) is present, as determined by the predominantly negative QRS complex in lead I.
Regarding assessment for chamber enlargement (and the explanation of the title of this ECG Review, plus the answer to our clinical question)—we suspect that this patient has four chamber enlargement. The tall peaked (pointed) P wave in standard lead II suggests right atrial enlargement (RAE). The notched P wave in lead I and the fairly deep (albeit pointed) negative component to the P wave in lead V1 suggests that there may also be left atrial enlargement (LAE). The surprisingly tall R wave in lead V6 (that exceeds 18 mm) is a less commonly invoked voltage criterion for left ventricular hypertrophy (LVH), but one that is probably accurate given the overall clinical picture. Finally, we suspect right ventricular hypertrophy (RVH). Admittedly, QRS morphology in standard leads I, II, and III is consistent with left posterior hemiblock (LPHB). However, the constellation of RAD, RAE and an rSr’ pattern in lead V1 is better explained by proposing RVH. Possible explanation for this patient’s dyspnea (in view of the ECG findings of sinus tachycardia and four-chamber enlargement) include heart failure from dilated congestive cardiomyopathy and/or pulmonary hypertension from pulmonary emboli or end-stage pulmonary disease. Examples of dextrocardia and lead misplacement were seen in the two previous ECG Reviews (Intern Med Alert 1999;21:184; Intern Med Alert 1999;21:168). Despite predominant negativity in lead I of this tracing, the reasons we don’t suspect lead misplacement or dextrocardia here are: 1) that a small positive deflection (r wave) is seen in lead I of this tracing (no r wave at all was seen in either of the two previous ECG Reviews); 2) both the P wave and T wave are upright in lead I here; 3) an upright P wave is seen in lead II; and 4) there is normal R wave progression in the precordial leads.
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